Abstract
Hydrogen sulfide (H2S) can protect the liver against ischemia-reperfusion (I/R) injury. However, it is unknown whether H2S plays a role in the protection of hepatic I/R injury in both young and old patients. This study compared the protective effects of H2S in a rat model (young and old animals) of I/R injury and the mechanism underlying its effects. Young and old rats were assessed following an injection of NaHS. NaHS alone reduced hepatic I/R injury in the young rats by activating the nuclear erythroid-related factor 2 (Nrf2) signaling pathway, but it had little effect on the old rats. NaHS pretreatment decreased miR-34a expression in the hepatocytes of the young rats with hepatic I/R. Overexpresion of miR-34a decreased Nrf-2 and its downstream target expression, impairing the hepatoprotective effect of H2S on the young rats. More importantly, downregulation of miR-34a expression increased Nrf-2 and the expression of its downstream targets, enhancing the effect of H2S on hepatic I/R injury in the old rats. This study reveals the different effects of H2S on hepatic I/R injury in young and old rats and sheds light on the involvement of H2S in miR-34a modulation of the Nrf-2 pathway.
Highlights
Hepatic warm ischemia-reperfusion (I/R) injury is a dynamic process that frequently occurs during a variety of clinical situations, including liver transplantation and liver surgery [1]
The present study explored the hepatoprotective effect of H2S on young (3 months) and old rats (20 months)
We found that NaHS alone could reduce hepatic I/R injury in young rats, but it had little effect on hepatic I/R injury in old rats
Summary
Hepatic warm ischemia-reperfusion (I/R) injury is a dynamic process that frequently occurs during a variety of clinical situations, including liver transplantation and liver surgery [1]. A series of events, such as the formation of reactive oxygen species (ROS), depletion of ATP, production of inflammatory mediators, and apoptosis of hepatocytes are involved in the pathophysiology of hepatic I/R [2]. Effective treatment of hepatic I/R injury is difficult. H2S has been reported to protect these tissues against I/R injury by maintaining mitochondrial function, inhibiting proinflammatory factors, neutralizing ROS and reducing apoptosis [6]. Treatment with H2S can be via inhalation of H2S or administration of NaHS by intravenous injection. It is difficult to control the concentration of inhaled H2S, resulting in potential toxicity to animals [7]. The administration of NaHS by intravenous injection has become the common treatment method in I/R injury because the concentration can be controlled [8]
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